Home General Physiology and Biophysics 2024 General Physiology and Biophysics Vol.43, No.4, p. 301–312, 2024

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
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General Physiology and Biophysics Vol.43, No.4, p. 301–312, 2024

Title: FUS-stabilized USP35 promotes growth, invasion and angiogenesis in NSCLC through deubiquitinating VEGFA
Author: Wei Li, Jianying Li, Wuhong Zheng, Jia Cheng, Xiaowei Zhang, Bingjing Yang, Jimin Dong, Xiangfei Sun
Abstract: Vascular endothelial growth factor A (VEGFA) is an important regulator for non-small cell lung cancer (NSCLC). Our study aimed to reveal its upstream pathway to provide new ideas for developing the therapeutic targets of NSCLC. The mRNA and protein levels of VEGFA, ubiquitin-specific peptidase 35 (USP35), and FUS were determined by quantitative real-time PCR and Western blot. Cell proliferation, apoptosis, invasion and angiogenesis were detected using CCK8 assay, EdU assay, flow cytometry, transwell assay and tube formation assay. The interaction between USP35 and VEGFA was assessed by Co-IP assay and ubiquitination assay. Animal experiments were performed to assess USP35 and VEGFA roles in vivo. VEGFA had elevated expression in NSCLC tissues and cells. Interferences of VEGFA inhibited NSCLC cell proliferation, invasion, angiogenesis, and increased apoptosis. USP35 could stabilize VEGFA protein level by deubiquitination, and USP35 knockdown suppressed NSCLC cell growth, invasion and angiogenesis via reducing VEGFA expression. FUS interacted with USP35 to promote its mRNA stability, thereby positively regulating VEGFA expression. Also, USP35 silencing could reduce NSCLC tumorigenesis by downregulating VEGFA. FUS-stabilized USP35 facilitated NSCLC cell growth, invasion and angiogenesis through deubiquitinating VEGFA, providing a novel idea for NSCLC treatment.
Keywords: Non-small cell lung cancer — VEGFA — USP35 — FUS
Published online: 29-Jun-2024
Year: 2024, Volume: 43, Issue: 4 Page From: 301, Page To: 312
doi:10.4149/gpb_2024010


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